| pubmed-article:20089077 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20089077 | lifeskim:mentions | umls-concept:C0009506 | lld:lifeskim |
| pubmed-article:20089077 | lifeskim:mentions | umls-concept:C0384648 | lld:lifeskim |
| pubmed-article:20089077 | lifeskim:mentions | umls-concept:C0026724 | lld:lifeskim |
| pubmed-article:20089077 | lifeskim:mentions | umls-concept:C0021390 | lld:lifeskim |
| pubmed-article:20089077 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:20089077 | lifeskim:mentions | umls-concept:C1515670 | lld:lifeskim |
| pubmed-article:20089077 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20089077 | pubmed:dateCreated | 2010-6-18 | lld:pubmed |
| pubmed-article:20089077 | pubmed:abstractText | Recent studies have demonstrated that the complement system participates in the regulation of T cell functions. To address the local biosynthesis of complement components in inflammatory bowel disease (IBD) mucosa, we investigated C3 and interleukin (IL)-17 mRNA expression in mucosal samples obtained from patients with IBD. The molecular mechanisms underlying C3 induction were investigated in human colonic subepithelial myofibroblasts (SEMFs). IL-17 and C3 mRNA expressions in the IBD mucosa were evaluated by real-time polymerase chain reaction. The C3 levels in the supernatant were determined by enzyme-linked immunosorbent assay. IL-17 and C3 mRNA expressions were elevated significantly in the active lesions from ulcerative colitis (UC) and Crohn's disease (CD) patients. There was a significant positive correlation between IL-17 and C3 mRNA expression in the IBD mucosa. IL-17 stimulated a dose- and time-dependent increase in C3 mRNA expression and C3 secretion in colonic SEMFs. The C3 molecules secreted by colonic SEMFs were a 115-kDa alpha-chain linked to a 70-kDa beta-chain by disulphide bonds, which was identical to serum C3. The IL-17-induced C3 mRNA expression was blocked by p42/44 mitogen-activated protein kinase (MAPK) inhibitors (PD98059 and U0216) and a p38 MAPK inhibitor (SB203580). Furthermore, IL-17-induced C3 mRNA expression was inhibited by an adenovirus containing a stable mutant form of I kappaB alpha. C3 and IL-17 mRNA expressions are enhanced, with a strong correlation, in the inflamed mucosa of IBD patients. Part of these clinical findings was considered to be mediated by the colonic SEMF response to IL-17. | lld:pubmed |
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| pubmed-article:20089077 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20089077 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20089077 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20089077 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20089077 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20089077 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:20089077 | pubmed:issn | 1365-2249 | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:TakeuchiKK | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:SugiharaTT | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:FujiyamaYY | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:TsujikawaTT | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:AndohAA | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:ImaedaHH | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:KoboriAA | lld:pubmed |
| pubmed-article:20089077 | pubmed:author | pubmed-author:AmagaseKK | lld:pubmed |
| pubmed-article:20089077 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20089077 | pubmed:volume | 160 | lld:pubmed |
| pubmed-article:20089077 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20089077 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20089077 | pubmed:pagination | 386-93 | lld:pubmed |
| pubmed-article:20089077 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
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